Effects of upregulation of Id3 in human lung adenocarcinoma cells on proliferation, apoptosis, mobility and tumorigenicity

Ff, Chen; Y, Liu; Wang, F; Xj, Pang; Cd, Zhu; Xu, Mei; Wang, Yu; Xj, Li

doi:10.1038/cgt.2015.38

Cited by 14 publications

(12 citation statements)

References 39 publications

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“…A549 human lung adenocarcinoma epithelial cells and that ectopic overexpression of Id3 in A549 cells inhibited their proliferation and induced apoptosis in vitro, as well as reducing tumor growth in vivo (13,14). These results suggested that Id3, as an upstream gene of the apoptotic signaling cascade, can induce cell apoptosis.…”

Section: Upregulation Of Id3 Inhibits Cell Proliferation and Induces mentioning

confidence: 83%

“…Numerous studies have assessed the role of Id3 in various cancer types (25,26). Previous studies by our group have shown that upregulation of Id3 inhibited the proliferation and induced apoptosis in A549 cells in vitro and in vivo (13,14), while further study is required to determine the underlying mechanisms. Therefore, ectopic expression of Id3 may represent a novel strategy for treating NSCLC.…”

Section: Discussionmentioning

confidence: 96%

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Upregulation of Id3 inhibits cell proliferation and induces apoptosis in A549/DDP human lung cancer cells in vitro

Chen

Zhao

Wang

et al. 2016

Molecular Medicine Reports

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Inhibitor of DNA binding (Id)3 is a member of the Id multigene family of dominant‑negative helix‑loop-helix transcription factors, which function as oncogenes or tumor suppressors in human cancers. Its upregulation was recently shown to have inhibitory effects on lung cancer, which is the leading cause of cancer‑associated mortality worldwide. As drug resistance represents a major bottleneck of cancer therapy, the present study assessed the ability of Id3 to inhibit cisplatin‑resistant A549 lung adenocarcinoma cells (A549/DDP). A549/DPP cells were transiently transfected with enhanced green fluorescence protein overexpression plasmid (pEGFP) or Id3 overexpression plasmid (Id3/pEGFP), which was confirmed by confocal fluorescence microscopy, PCR and western blot analysis. The effects of Id3 on the viability and apoptosis of A549/DDP were determined using an MTT assay, fluorescence microscopy with Hoechst 33258 staining and flow cytometry following Annexin V/propidium iodide double staining. The results revealed that overexpression of Id3 significantly inhibited the proliferation and viability of A549/DDP cells in a time‑dependent manner. Furthermore, overexpression of Id3 significantly increased the apoptotic rate of A549/DDP cells from 2.73 to 16.92%, confirming the implication of Id3 in the negative control of tumour growth. The results of the present study revealed that overexpression of Id3 may serve as a novel strategy for inhibiting cisplatin‑sensitive lung cancer. Further experiments will be performed to determine whether Id3 overexpression could enhance the sensitivity of lung cancer cells to DDP.

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Section: Upregulation Of Id3 Inhibits Cell Proliferation and Induces mentioning

confidence: 83%

Section: Discussionmentioning

confidence: 96%

Upregulation of Id3 inhibits cell proliferation and induces apoptosis in A549/DDP human lung cancer cells in vitro

Chen

Zhao

Wang

et al. 2016

Molecular Medicine Reports

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“…It is reported that overexpressed Id3 inhibited cell proliferation and induced apoptosis and may be a potential target for tumor suppression [52]. Here, downregulated Id3 may activate cell proliferation, such as T cell, macrophages and may be a potential drug for immunodeficiency therapy.…”

Section: Effects Of Fenps On the Expression Of Id Genesmentioning

confidence: 99%

Research on Nanotoxicity of an Iron Oxide Nanoparticles and Potential Application

Zhang¹,

Xie²,

Liu³

et al. 2017

Toxicol Open Access

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The iron oxide nanoparticles (FeNPs) are widely used in biomedicine for good biocompatibility. To promote its safe application, any potential nanotoxicity should be thoroughly and carefully investigated. This paper systematically summarizes our lab's research on the nanotoxicity of iron oxide nanoparticles coated with dimercaptosuccinic acid (DMSA), including the effects of FeNPs on viability, apoptosis, cycle, and oxidative stress at cell level. In vitro studies revealed that the FeNPs showed obvious apoptosis of human acute monocyte cells (THP-1) and human hepatoma cells (HepG2) at the highest concentration. FeNPs resulted in common and cell typespecific nanotoxicities of the FeNPs to both human and mouse cells at the gene, disturbed cell's iron and osmosis homeostasis by the internalization of FeNPs through releasing iron ion in cells, resulted in cytotoxicity of DMSA as coating molecules of FeNPs and the inhibitor of DNA binding/differentiation (Id) related nanotoxicity of FeNPs at gene level. The studies of our lab shed many new insights into the nanotoxicity of the nanoparticle. Furthermore, the toxicity may play more value if it is guided and applied reasonably, such as iron supplement, anti-oxidation, and immunotherapy.

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“…The EA.hy926 cells were cultivated in DMEM supplemented with 10% FBS and 1% penicillin/streptomycin, and incubated at 37°C in a 5% CO 2 -humidified atmosphere. 19,20 The B16 cells were cultured under the same conditions, in RPMI 1640 medium. Cells were subcultured at ~80% confluence.…”

mentioning

confidence: 99%

“…Finally, affinity kinetic data between CS-ES2-AF and ES2-AF to CD44 were tested by a single-loop experiment according to the wizard program in the operating system, and the affinity of the two drugs for CD44 was compared. 19,[32][33][34] Bioimaging of FITc-labeled cs-es2-aF conjugate…”

mentioning

confidence: 99%

<p>Characterization and bioactivity of self-assembled anti-angiogenic chondroitin sulphate-ES2-AF nanoparticle conjugate</p>

Liang¹,

Sun²,

Wang³

et al. 2019

IJN

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Background In the past few years, significant progress has been made in inhibiting neovascularization at the tumor site, cutting off the nutrient supply of the tumor, and inhibiting tumor growth and metastasis. However, many proteins/peptides have the disadvantage of poor stability, short half-life, and uncertain targeting ability. Chemical modification can be used to overcome these disadvantages; many polyethylene glycol-modified proteins/peptides have been approved by US FDA. The purpose of this study was to obtain a novel anti-angiogenic chondroitin sulfate (CS)-peptide nanoparticle conjugate with efficient anti-neovascularization and tumor targeting ability and an acceptable half-life. Materials and methods The CS-ES2-AF nanoparticle conjugate was synthesized and characterized using 1 H-nuclear magnetic resonance spectroscopy, transmission electron microscopy, and particle size and zeta potential analyzer. The anti-angiogenic ability was studied using MTT, migration, tube formation, and chick chorioallantoic membrane assays. The targeting ability of CS-ES2-AF was studied by ELISA, surface plasmon resonance, and bioimaging. The pharmacokinetics was also studied. Results The CS-ES2-AF could self-assemble into stable nanoparticles in aqueous solution, which significantly enhances its anti-neovascularization activity, tumor targeting more explicit, and prolongs its half-life. Conclusion CS is an effective protein/peptide modifier, and CS-ES2-AF displayed good potential in tumor targeting therapy.

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Effects of upregulation of Id3 in human lung adenocarcinoma cells on proliferation, apoptosis, mobility and tumorigenicity

Cited by 14 publications

References 39 publications

Upregulation of Id3 inhibits cell proliferation and induces apoptosis in A549/DDP human lung cancer cells in vitro

Upregulation of Id3 inhibits cell proliferation and induces apoptosis in A549/DDP human lung cancer cells in vitro

Research on Nanotoxicity of an Iron Oxide Nanoparticles and Potential Application

<p>Characterization and bioactivity of self-assembled anti-angiogenic chondroitin sulphate-ES2-AF nanoparticle conjugate</p>

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